Gum acacia mitigates genetic damage in adenine-induced chronic renal failure in rats

• Published in: European journal of clinical investigation 2015-12, Vol.45 (12), p.1221-1227
• Main Authors: Ali, B.H., Al Balushi, K., Al-Husseini, I., Mandel, P., Nemmar, A., Schupp, N., Ribeiro, D.A.
• Format: Article
• Language: English
• Subjects: Adenine; Adenine - toxicity; Animals; chronic renal failure; Comet Assay; Comet test; Deoxyguanosine - analogs & derivatives; Deoxyguanosine - urine; DNA damage; DNA Damage - drug effects; DNA Damage - genetics; Guanine - analogs & derivatives; Guanine - urine; Guanosine - analogs & derivatives; Guanosine - urine; gum acacia; Gum Arabic - pharmacology; Kidney Failure, Chronic - chemically induced; Kidney Failure, Chronic - genetics; Kidney Failure, Chronic - prevention & control; Kidney Function Tests; Male; Random Allocation; rats; Rats, Wistar; Renal Agents - pharmacology
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1111/eci.12501

Background Subjects with chronic renal failure (CRF) exhibit oxidative genome damage, which may predispose to carcinogenesis, and Gum acacia (GumA) ameliorates this condition in humans and animals. We evaluated here renal DNA damage and urinary excretion of four nucleic acid oxidation adducts namely 8‐oxoguanine (8‐oxoGua), 8‐oxo‐7,8‐dihydro‐2′‐deoxyguanosine (8‐oxodG), 8‐oxoguanosine (8‐oxoGuo) and 8‐hydroxy‐2‐deoxyguanisone (8‐OHdg) in rats with adenine (ADE)‐induced CRF with and without GumA treatment. Materials and Methods Twenty‐four rats were divided into four equal groups and treated for 4 weeks. The first group was given normal food and water (control). The second group was given normal food and GumA (15% w/v) in drinking water. The third group was fed powder diet containing adenine (ADE) (0·75% w/w in feed). The fourth group was fed like in the third group, plus GumA in drinking water (15%, w/v). Results ADE feeding induced CRF (as measured by several physiological, biochemical and histological indices) and also caused a significant genetic damage and significant decreases in urinary 8‐oxo Gua and 8‐oxoGuo, but not in the other nucleic acids. However, concomitant GumA treatment reduced the level of genetic damage in kidney cells as detected by Comet assay and significantly reversed the effect of adenine on urinary 8‐oxoGuo. Conclusions Treatment with GumA is able to mitigate genetic damage in renal tissues of rats with ADE‐induced CRF.